Acute renal failure (ARF) refers to a deterioration in renal function sufficient to result in the accumulation of nitrogenous wastes in the body. In general, patients suffering from acute renal injury can regain kidney function if the condition is diagnosed early and treated promptly.
Chronic renal failure, however, involves irreversible kidney damage, typically progressive and permanent destruction of nephrons. Early diagnosis and treatment of acute renal failure can in some cases arrest or prevent progression to a chronic condition.
Approximately five percent of all hospitalized patients develop acute renal failure; in some clinical settings, such as intensive care units, ARF can occur in up to 20 percent of the patients. Acute renal failure may be due to prerenal, renal or postrenal causes. About 40 to 80 percent of all cases of acute renal failure are caused by decreased renal perfusion (prerenal azotemia), often resulting from varied conditions or events such as gastrointestinal hemorrhage, burns, diarrhea, severe congestive heart failure, pancreatitis, or sepsis. Postrenal causes, such as bladder neck constriction, account for about 10 percent of all cases of ARF while renal causes include disorders such as thrombosis, emboli, and vasculitis. Additionally, two types of common pharmacologic agents, non-steroidal anti-inflammatory agents (NSAID's) and angiotensin converting enzyme inhibitors may cause ARF in predisposed patients. Cross sectional studies have also found that aging is typically accompanied by a decline in renal function (Harrison).
ARF is typically detected by determination of glomerular filtration rate (GFR) or blood urea nitrogen or serum creatinine levels. GFR is the rate of ultrafiltration of plasma across the walls of the glomerular capillaries and measurement of total GFR of both kidneys provides a sensitive index of overall renal excretory function. Normal renal excretory function is indicated by a GFR of about 125 mL/min (180 L/day), although when renal excretory capacity is impaired, total GFR declines. Often, measurements of urea and creatinine concentrations are used to assess the glomerular filtration rate. Both substances are produced at a relatively constant rate by the liver and muscles; an increase in their respective serum concentrations occurs as GFR declines due to the fact that both compounds undergo complete glomerular filtration and are not reabsorbed by the renal tubules. Creatinine provides a more reliable index of GFR than urea because urea can back diffuse more completely from tubule lumen to peritubular blood than creatinine. Thus, blood urea nitrogen levels are typically higher than serum creatinine levels; a normal ratio of blood urea nitrogen to serum creatinine is about 10.
Chemical analysis of both urine and serum samples are useful indicators of ARF. For example, the range of urine osmolalities that can be achieved by an individual with normal-functioning kidneys (40 to 1200 mosmol/kg) is much larger than the range achievable in diseased kidneys (250-350 mosmol/kg). Typically, acute renal failure is characterized by urine osmolalities of below about 400 mosmol/kg, urine sodium concentrations above about 40 mmol/L, a ratio of urine-to-plasma creatinine levels below 20, and a fractional excretion of filtered sodium, defined as the ratio of urine sodium concentration/serum sodium concentration to urine creatinine concentration/serum creatinine concentration multiplied by 100, of about 2 (Harrison).
As mentioned above, the early effective treatment of ARF can arrest the progression of the condition to chronic renal failure, where permanent kidney damage occurs.